The objective of this research is to determine the mechanism of the estradiol-induced stimulation of glucose and amino acid uptake by ovariectomized rat uterus. Stimulation begins within 30 min of estradiol treatment, which is before generalized protein synthesis begins. While protein synthesis of transport proteins may be important in this process, it is possible that estradiol-induced membrane alterations may also be significant, especially during the first 6 hr after estradiol treatment. To test this hypothesis, the following aims have been established. They are: 1. To characterize the estradiol-induced changes in uterine plasma membrane phospholipids. 2. To determine the effect of the manipulation of uterine plasma membrane composition on the estradiol-induced increase in glucose and amino acid uptake. 3. To determine the effect of estradiol on the amount of uterine glucose transport proteins in plasma membranes. The approach will be to determine the effects of estradiol on uterine phospholipid fatty acids. Preliminary results show significant changes in the amount of several fatty acids in the phospholipids of uterine plasma membranes. It will be shown whether essential fatty acid deprivation of ovariectomized rats will prevent the estradiol effects on glucose and amino acid uptake. It will be determined if estradiol-induced changes in transport can be mimicked or prevented by modification of uterine cell membranes by insertion of various lipid perturbants. The contribution of protein synthesis to the estradiol effects will be measured by monitoring the synthesis of glucose transport proteins by affinity labeling. The effect of protein synthesis inhibitors will be correlated with the estradiol effect on uptake. This research will describe the effects of estradiol on uterine plasma membrane function and may produce new information about the stimulation of protein synthesis at an earlier time after estradiol treatment than at which it is usually studied.